Evidence map›Paper›PMID 29098549›Full record

ArticleDigestive diseases and sciences2017

The GAS5/miR-222 Axis Regulates Proliferation of Gastric Cancer Cells Through the PTEN/Akt/mTOR Pathway.

Yanhua Li, Junjiao Gu, Hong Lu

Abstract read
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In one paragraph

Article in Digestive diseases and sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.6field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
  2. Review
  3. Epigenetic Regulation by lncRNA GAS5/miRNA/mRNA Network in Human Diseases.International journal of molecular sciences · 2025
    Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Expression Profiles of Long Non-Coding RNADiagnostics (Basel, Switzerland) · 2021
    Article
  11. Review
  12. Cancer management and research · 2021
    Article
  13. Review
  14. The Non-Coding RNAInternational journal of molecular sciences · 2020
    Review
  15. Review
  16. Article
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  18. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Yanhua LiDepartment of Oncology, Huaihe Hospital of Henan University, No. 8 Baobei Road, Kaifeng, 475000, Henan, People's Republic of China.
Junjiao GuDepartment of Oncology, Huaihe Hospital of Henan University, No. 8 Baobei Road, Kaifeng, 475000, Henan, People's Republic of China.
Hong LuDepartment of Oncology, Huaihe Hospital of Henan University, No. 8 Baobei Road, Kaifeng, 475000, Henan, People's Republic of China. honglu6512@163.com.
Henan University Huaihe Hospital and Huaihe Clinical Institute · CN

Funding

Science & Technology Department of Henan Province 9412016Y1403
6 · The paper itself

Abstract

backgroundSeveral lines of evidence have indicated that growth arrest-specific transcript 5 (GAS5) functions as a tumor suppressor and is aberrantly expressed in multiple cancers. GAS5 was found to be downregulated in gastric cancer (GC) tissues, and ectopic expression of GAS5 inhibited GC cell proliferation.

aimsThe present study aimed to explore the underlying mechanisms of GAS5 involved in GC cell proliferation.

methodsGAS5 and miR-222 expressions in GC cell lines were estimated by quantitative real-time polymerase chain reaction. The effects of GAS5 and miR-222 on GC cell proliferation were assessed by MTT assay and 5-bromo-2-deoxyuridine (BrdU) incorporation assays. The interaction between GAS5 and miR-222 was confirmed by luciferase reporter assay and RNA immunoprecipitation assay. The protein levels of the phosphatase and tensin homolog (PTEN), phosphorylated protein kinase B (Akt) (p-Akt), Akt, phosphorylated mammalian target of rapamycin (mTOR) (p-mTOR), and mTOR were determined by western blot.

resultsGAS5 was downregulated and miR-222 was upregulated in GC cells. GAS5 directly targeted and suppressed miR-222 expression. GAS5 overexpression and miR-222 inhibition suppressed cell proliferation, increased PTEN protein level and decreased p-Akt and p-mTOR protein levels in GC cells while GAS5 knockdown and miR-222 overexpression exhibited the opposite effects. Moreover, mechanistic analyses revealed that GAS5 regulated GC cell proliferation through the PTEN/Akt/mTOR pathway by negatively regulating miR-222.

conclusionsGAS5/miR-222 axis regulated proliferation of GC cells through the PTEN/Akt/mTOR pathway, which facilitated the development of lncRNA-directed therapy against this deadly disease.

Indexed as

Cell Line, TumorGene Expression Regulation, NeoplasticHumansMicroRNAsProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseRNA, Long NoncodingStomach NeoplasmsTOR Serine-Threonine KinasesGAS5 long non-coding RNA, humanMicroRNAsMIRN22 microRNA, humanMTOR protein, humanProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanRNA, Long NoncodingTOR Serine-Threonine KinasesGAS5Gastric cancermiR-222ProliferationPTEN/Akt/mTOR pathway

Identifiers

PMID29098549
OpenAlexW2766621857

What OpenQuestion holds

Textmetadata
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.